These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Fatty Acid Oxidation and Its Relation with Insulin Resistance and Associated Disorders.
    Author: Lopaschuk GD.
    Journal: Ann Nutr Metab; 2016; 68 Suppl 3():15-20. PubMed ID: 27931032.
    Abstract:
    Alterations in muscle fatty acid metabolism have been implicated in mediating the severity of insulin resistance. In the insulin resistant heart fatty acids are favored as an energy source over glucose, which is thus associated with increased fatty acid oxidation, and an overall decrease in glycolysis and glucose oxidation. In addition, excessive uptake and beta-oxidation of fatty acids in obesity and diabetes can compromise cardiac function. In animal studies, mice fed a high fat diet (HFD) show cardiac insulin resistance in which the accumulation of intra-myocardial diacylglycerol has been implicated, likely involving parallel signaling pathways. A HFD also results in accumulation of fatty acid oxidation byproducts in muscle, further contributing to insulin resistance. Carnitine acetyltransferase (CrAT) has an essential role in the cardiomyocyte because of its need for large amounts of carnitine. In the cardiomyocyte, carnitine switches energy substrate preference in the heart from fatty acid oxidation to glucose oxidation. This carnitine-induced switch in fatty acid oxidation to glucose oxidation is due to the presence of cytosolic CrAT and reverse CrAT activity. Accordingly, inhibition of fatty acid oxidation, or stimulation of CrAT, may be a novel approach to treatment of insulin resistance.
    [Abstract] [Full Text] [Related] [New Search]